General Terms of Use

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You are currently connected to a website named “Exploring (rare) cholestasis” dedicated to providing information about the possible causes of cholestasis and jaundice in newborns and children and about hereditary primary bile acid synthesis disorders. This website was developed and put online by Laboratoires CTRS.

This website is reserved for healthcare professionals and is intended to provide information about possible rare causes of cholestasis and jaundice in newborns and children and about hereditary primary bile acid synthesis disorders.

1. TERMS OF USE

Please read these General Terms of Use carefully. They govern the terms of use of the rarecholestasis.com website, which you accept solely by consulting our website.

This website is reserved exclusively for providing information to healthcare professionals.

If you do not agree to these General Terms of Use, please leave our website. Laboratoires CTRS reserves the right to modify or have modified the General Terms of Use, at any time and without notice, as well as the information presented on this website. We draw your attention to the fact that you need to consult these General Terms of Use regularly, taking into account the most recent update date indicated on the website, in order to stay informed of any changes that Laboratoires CTRS may make to them.

2. PUBLISHER

Laboratoires CTRS is a French simplified joint stock company (‘S.A.S.’) with a share capital of € 93,116. Its head office is located at 63, rue de l’Est, 92100 Boulogne-Billancourt (France) and it is registered in the Nanterre Trade and Companies Register under number 816 420 301.

Publication Director: Antoine Ferry, Chairman/CEO of Laboratoires CTRS

Website Manager: EVAIN Laetitia, Project Manager for Laboratoires CTRS

Site hosting: OVH 2 Rue Kellermann, 59100 Roubaix, France

3. PURPOSE OF THE WEBSITE

This website was created to supply healthcare professionals with general information about possible rare causes of cholestasis and jaundice in newborns and children and about hereditary primary bile acid synthesis disorders.

The information contained on this website, intended for healthcare professionals, is provided to you for information purposes only and is not intended in any way to:

4. DISCLAIMER OF WARRANTIES

The information and data contained in this website or any other website are provided “as is” without any warranty of any kind, express or implied. Users of the website acknowledge that they are solely responsible for any use they may make of the information provided on the website. Consequently, Laboratoires CTRS cannot be held liable for any direct or indirect damages of any kind whatsoever resulting wholly or partly from the use of the information on the website.

If you access and use the contents of the website, you do so at your own risk.
Laboratoires CTRS makes every effort to keep the information on this website up to date. However, Laboratoires CTRS guarantees neither its completeness nor its accuracy, whatever the information provided.

You acknowledge that: (i) it is technically impossible to ensure that this website is free of errors and that Laboratoires CTRS does not warrant it; (ii) errors may make the website temporarily unavailable; and (iii) the operation of the website may be affected by events and/or circumstances beyond the control of Laboratoires CTRS such as, for example, a breakdown or failure of transmission and communication between you and Laboratoires CTRS, and between Laboratoires CTRS and other networks.

Laboratoires CTRS and/or its service-providers may at any time change or discontinue temporarily or permanently all or part of the website to perform maintenance operations and/or improve or change the website. Laboratoires CTRS is not responsible for any website changes, suspensions or interruptions.

5. LIMITATION OF LIABILITY

Laboratoires CTRS cannot be held liable, in any way whatsoever:

6. INTELLECTUAL PROPERTY

The documents contained in and the elements created for the website are the exclusive property of Laboratoires CTRS, or of the third parties that have authorised Laboratoires CTRS to quote them.
In addition, all the images and texts appearing on this website are the exclusive property of Laboratoires CTRS and may only be used in accordance with the conditions set out below.

With effect from your acceptance of these General Terms of Use, you may download, display or print the information contained on this website for exclusively personal and private use, for non-commercial purposes and without changing or altering the legal information relating to copyright, trademarks, or other property rights and provided the following copywrite notice is reproduced on each full or partial copy of the content of the website: “Copyright © CTRS 2020 – all rights reserved”.

Any use other than that indicated above, without the prior written permission of Laboratoires CTRS, is strictly prohibited and constitutes a breach of copyright. Laboratoires CTRS does not grant you any other rights other than those described above, nor any other licence of intellectual or industrial property, or know-how which it owns or which it uses.
Laboratoires CTRS reserves the right to take legal action for any infringement of its intellectual property rights.

7. INFORMATION ORIGINATING FROM THIRD PARTIES

The website also contains, with the agreement of third parties, information originating from third parties, and links to other websites. Laboratoires CTRS tries to reference only sites that comply with applicable legislation.
This information and these links are provided to you purely for information purposes and for your convenience.
Since Laboratoires CTRS is not in a position to carry out any controls on the information supplied by third parties or published on third-party websites, Laboratoires CTRS is unable to endorse this information and cannot be held responsible for their content, which you access under your entire responsibility.

Laboratoires CTRS reserves the right to delete any content or link that it considers objectionable, or following the knowledge of a dispute relating to a given content or link.
The website may offer you opinions expressed by experts consulted in a particular field in relation to the content of the website or excerpts of press articles. Such information represents only the opinion of the consulted expert or of the journal, and not necessarily the opinion of Laboratoires CTRS; Laboratoires CTRS cannot be held responsible for the accuracy and completeness of the information and opinions contained in such material.

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Laboratoires CTRS®, AMFE

8. LINKS TO OTHER EXTERNAL OR THIRD-PARTY WEBSITES

Laboratoires CTRS’s website may contain hypertext links to third-party websites. The sole purpose of these links to other websites is to facilitate your visit to our website. In any event, and particularly because of the volatile nature of the information available on the internet, Laboratoires CTRS cannot control the nature or the content of the resources constituted by these external sources and, consequently, cannot be held responsible for the use or unavailability of the third-party websites, their content, the advertising and other elements available on these third-party websites which can be accessed via the Laboratoires CTRS website.

Laboratoires CTRS has no means of controlling the content of these third-party websites, which remain completely independent of Laboratoires CTRS. Furthermore, the existence of a link between the Laboratoires CTRS website and a third-party website does not mean that Laboratoires CTRS approves in any way whatsoever the content of the website and the use that could be made of it.

In addition, it is your responsibility to take the necessary precautions to avoid any contamination of the website, particularly by one or more viruses and/or other parasites.
External websites may contain hypertext links to the Laboratoires CTRS website. Such a link does not mean that there is any connection between Laboratoires CTRS and the third-party website. In any event, Laboratoires CTRS cannot be held in any way responsible for the unavailability of such websites and Laboratoires CTRS does not review, check or approve and cannot be held responsible for the content, advertising, products or other items available on or via these websites.

9. PROTECTION OF PERSONAL DATA

A) COLLECTION OF ANONYMOUS DATA

No personal information regarding your identity is collected without your knowledge. However, during visits to the website, certain user data is collected automatically:

Consequently, Laboratoires CTRS collects anonymous user data (or anonymous information) from this website, such as the pages that you visit and the searches you undertake. These data are not nominative, because in no case do they allow personal identification of the website. We use this anonymous information to help us improve the content of our websites and obtain overall statistics on your visits. These statistics may be compiled by third parties; in such cases, they have an obligation of confidentiality.

B) USE OF COOKIES

This anonymous information is collected in particular by means of cookies. See section 11 below for more information.

C) COLLECTION OF NOMINATIVE DATA

This website does not gather any nominative or personal data.

D) SECURITY

To protect the personal information you provide, Laboratoires CTRS uses security technologies. However, the internet is an open network, so Laboratoires CTRS cannot guarantee that third parties will not intercept or reroute this personal information. Laboratoires CTRS will not be liable to you should this be the case.
Laboratoires CTRS offers no guarantee that the websites that are linked to it follow the same measures for the protection of personal data as those set out in these General Terms. You should therefore check their data protection measures yourself if you provide personal information on these websites.

10. JURISDICTION

The website and its content are governed by French law and any dispute relating thereto shall be subject to the jurisdiction of the French courts.

11. USE OF COOKIES AND CONNECTION INDICATORS

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You have the option, if you so wish, to oppose the saving of these session ID cookies by configuring your browser accordingly. By its nature, this operation may modify or hinder your browsing on the website.

We do not have any control over the processes used by the social networks to collect information about your browsing on our website.
The issuing and use of cookies by these third parties are subject to their own privacy policies. We invite you to read these policies to identify the end use, namely for advertising, and the browsing information which they can collect through application plug-ins, and thereby make your own decision. In particular, these privacy protection policies must allow you to exercise your choices with these social networks, particularly the setting up of your user accounts for each of these networks.

Otherwise, you may refuse the use of these cookies by following the procedure indicated on your browser (see the procedure to be followed below), according to the terms that suit you best.
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CTRS-INSTIT-PLATEDUC-ONG15/20/07/20

Normal values:

Vitamin A: 30–120 μg/dL

Vitamin D: 20–100 ng/mL

Vitamin E: 5–20 μg/mL

Bilirubin metabolism5-7

Unconjugated
bilirubin

Bilirubin is mainly
produced from the
break down of red
blood cells.

Red cell breakdown
produces unconjugated
(“indirect”) bilirubin,
which circulates mostly
bound to albumin,
although some is
“free” and hence
able to enter the brain.

The terms “direct”
and “indirect” refer
to the way laboratories
measure the different
forms.

Unconjugated bilirubin
is metabolised in the
liver to produce
conjugated (“direct”)
bilirubin by uridine
diphosphate
glucuronosyltransferase.

The activity of this
enzyme only rises after
birth to reach adult like
values around the age
of three months.

Conjugation of bilirubin
increases its solubility
and facilitates its
secretion into bile.

Conjugated (“direct”)
bilirubin then passes
into the gut and is
largely excreted.

In the gastrointestinal
tract, bilirubin is modified
by digestive bacteria and
transformed into
urobilinogens . A large
portion remains in the
intestine and is
converted into stercobilin
(responsible for the
brown colour of faeces).
Some is reabsorbed into
the bloodstream and the
remainder is excreted in
the urine (urobilin is
responsible for the
yellow colour of urine).

Reticuloendothelial
system

Red blood cells

albumin

Haeme

Blood

“Indirect bilirubin”

“Direct bilirubin”

Liver

Intestine

Conjugated
bilirubin

Urobilinogens

Uridine
diphosphate
glucuronosyl-
transferase

Excreted in bile

Gut bacteria

Enterohepatic
circulation

Excreted in urine
(urobilin)

Excreted in faeces
(stercobilin)

Unconjugated
bilirubin-albumin
complex

​TH-BAS07EN/01/02/2024

Normal values:

Total bilirubin: 0-1.1 mg/dL

Vitamin A: 20-43 µg/dL

Vitamin E: 2.9 – 16.6 mg/L

Vitamin K1: 80-160 pg/mL

Normal values:

Serum calcium: 8.7 – 9.8 mg/dL

Serum phosphorous: 3.9 – 6.5 mg/dL

PTH: 15 – 65 pg/mL

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Enzymatic pathways of bile acid synthesis

classic pathway

adapted from Sundaram 20081 and Monte 20092

Cholesterol

Cholesterol 7α-hydroxylase
CYP7A1

3β-hydroxy-Δ5 -C27-steroid dehydrogenase
HSD3B7

Δ4-3-oxosteroid-5β-reductase
AKR1D1

Δ4-3-oxosteroid-5β-reductase
AKR1D1

3α-hydroxysteroid dehydrogenase
AKR1C4

Sterol 27-hydroxylase
CYP27A1

Bile acid CoA synthetase (BACS)
or very long chain acyl CoA
synthetase (VLCS)

Side-chain modification by
4 peroxisomal enzymes
(AMACR, BCOX, BDP, SCPx)

3α-hydroxysteroid dehydrogenase
AKR1C4

Sterol 27-hydroxylase
CYP27A1

Bile acid CoA synthetase (BACS)
or very long chain acyl CoA
synthetase (VLCS)

Side-chain modification by
4 peroxisomal enzymes
(AMACR, BCOX, BDP, SCPx)

Amino acid N-acyltransferase
(BAAT)

Amino acid N-acyltransferase
(BAAT)

7α-hydroxycholesterol

7α-hydroxy
4 cholesten-3-one

7α-12α-dihydroxy
-4 cholesten-3-one

7α-dihydroxy-5β-
cholestan-3-one

5β-cholestan-
3α,7α -diol

3α,7α-dihydroxy-5β-
cholestanoic acid (DHCA)

DHCA-CoA

Chenodeoxycholic
acid

Glyco or tauro-
chenodeoxycholic acid

Glyco or tauro-
cholic acid

Cholic acid

3α,7α,12α-trihydroxy-5β-
cholestanoic acid (THCA)

5β-cholestan-
3α,7α,12α-triol

7α-12α-dihydroxy-
5β-cholestan-3-one

THCA-CoA

Microsomes

Cytosol

Mitochondria

peroxisomes

hepatocyte

Endoplasmic
reticulum

Sterol 12α-hydroxylase
CYP8B1

AMARC: alpha methylacyl-CoA racemase

BCOX: Branched-chain acyl CoA oxydase

BDP: D-bifunctional protein hydratase 

SCPx: Sterol carrier protein

Alternative pathway

Cholesterol

Oxysterol 7α-hydroxylase
CYP7B1

3β-hydroxy-Δ5-C27-steroid dehydrogenase
HSD3B7

Side-chain modifications

Sterol 27-hydroxylase
CYP27A1

Amino acid N-acyltransferase
(BAAT)

3β-hydroxy-5-cholestanoic acid

3-oxo-7α-hydroxy-4-cholestanoic acid

3β,7α-dihydroxy-5-cholestanoic acid

Chenodeoxycholic acid

Glyco or tauro-
chenodeoxycholic acid

adapted from Sundaram 20081

1. Sundaram SS, Bove KE, Lovell MA, Sokol RJ. Mechanisms of disease: Inborn errors of bile acid synthesis. Nat Clin Pract Gastroenterol Hepatol 2008;5:456-68.

2. Monte MJ, Marin JJG, Antelo A, Vazquez-Tato J. Bile acids: chemistry, physiology, and pathophysiology. World J Gastroenterol 2009;15:804-16

​TH-BAS10EN/01/02/2024

 

REMINDER ABOUT BILE ACIDS

The bile acid family is a group of acid steroids synthesised from cholesterol in the liver. Although their best-known role is to aid with the emulsion, digestion and absorption of fats and liposoluble vitamins, other important physiological roles have been identified.1

On secretion of bile acids into bile canaliculi, osmotic pressure is created that accounts for the bile-acid-dependent fraction of bile flow. Bile acids stimulate biliary lipid secretion and form mixed micelles with biliary phospholipids, allowing the solubilisation of cholesterol and other lipophilic compounds in the bile. The mixed micelles also emulsify dietary fats in the intestines, facilitating their absorption.1

Bile acid synthesis

The primary bile acids, cholic acid and chenodeoxycholic acid are synthesised from cholesterol by an enzymatic cascade involving nearly 20 enzymes and two complementary chemical pathways, the classic “neutral” pathway and the alternative “acidic” pathway.2,3 Although the neutral pathway is believed to be the major pathway for bile acid synthesis in adults, in the first months of life the acidic pathway is thought to be more important.2,5 In humans and under normal conditions, the acidic pathway contributes little (approximately 10%) to the restitution of daily loss of bile acid.1 It may become the major bile acid biosynthetic pathway in patients with liver diseases.1

The primary bile acids produced include cholic acid (CA), which accounts for approximately 70% of the circulating pool of bile acids, and chenodeoxycholic acid (CDCA), which accounts for approximately 30% of the pool.4

Enzymatic pathways of bile acid synthesis

classic pathway

adapted from Sundaram 20083 and Monte 20091

Cholesterol

Cholesterol 7α-hydroxylase
CYP7A1

3β-hydroxy-Δ5 -C27-steroid dehydrogenase
HSD3B7

Δ4-3-oxosteroid-5β-reductase
AKR1D1

Δ4-3-oxosteroid-5β-reductase
AKR1D1

3α-hydroxysteroid dehydrogenase
AKR1C4

Sterol 27-hydroxylase
CYP27A1

Bile acid CoA synthetase (BACS)
or very long chain acyl CoA
synthetase (VLCS)

Side-chain modification by
4 peroxisomal enzymes
(AMACR, BCOX, BDP, SCPx)

3α-hydroxysteroid dehydrogenase
AKR1C4

Sterol 27-hydroxylase
CYP27A1

Bile acid CoA synthetase (BACS)
or very long chain acyl CoA
synthetase (VLCS)

Side-chain modification by
4 peroxisomal enzymes
(AMACR, BCOX, BDP, SCPx)

Amino acid N-acyltransferase
(BAAT)

Amino acid N-acyltransferase
(BAAT)

7α-hydroxycholesterol

7α-hydroxy
4 cholesten-3-one

7α-12α-dihydroxy
-4 cholesten-3-one

7α-dihydroxy-5β-
cholestan-3-one

5β-cholestan-
3α,7α -diol

3α,7α-dihydroxy-5β-
cholestanoic acid (DHCA)

DHCA-CoA

Chenodeoxycholic
acid

Glyco or tauro-
chenodeoxycholic acid

Glyco or tauro-
cholic acid

Cholic acid

3α,7α,12α-trihydroxy-5β-
cholestanoic acid (THCA)

5β-cholestan-
3α,7α,12α-triol

7α-12α-dihydroxy-
5β-cholestan-3-one

THCA-CoA

Microsomes

Cytosol

Mitochondria

peroxisomes

hepatocyte

Endoplasmic
reticulum

Sterol 12α-hydroxylase
CYP8B1

AMACR: alpha methylacyl-CoA racemase

BCOX: Branched-chain acyl CoA oxydase

BDP: D-bifunctional protein hydratase 

SCPx: Sterol carrier protein

The classic pathway, also known as the “neutral” pathway because its intermediate metabolites are neutral sterols, is the main pathway for bile acid synthesis.1-3 It is present only in the liver and synthesises cholic acid and chenodeoxycholic acid.1 This pathway consists of a cascade of reactions catalysed by enzymes located in microsomes, the cytosol, mitochondria and peroxisomes.1 The final step in the synthesis of bile acid is the conjugation of cholic acid and chenodeoxycholic acid to taurine or glycine.3

Alternative pathway

Cholesterol

Oxysterol 7α-hydroxylase
CYP7B1

3β-hydroxy-Δ5-C27-steroid dehydrogenase
HSD3B7

Side-chain modifications

Sterol 27-hydroxylase
CYP27A1

Amino acid N-acyltransferase
(BAAT)

3β-hydroxy-5-cholestanoic acid

3-oxo-7α-hydroxy-4-cholestanoic acid

3β,7α-dihydroxy-5-cholestanoic acid

Chenodeoxycholic acid

Glyco or tauro-
chenodeoxycholic acid

adapted from Sundaram 2008 and Monte 20091

The alternative pathway involves C27-hydroxylation of cholesterol by sterol 27-hydroxylase as the initial step: side-chain oxidation of cholesterol precedes steroid ring modification.1,3 Thus, acidic intermediate metabolites are formed: this is why this pathway is also known as the “acidic” pathway.1 It primarily produces chenodeoxycholic acid.3

Regulation of bile acid synthesis

Bile acid synthesis is tightly regulated to ensure homeostatic levels of cholesterol are produced and to provide adequate emulsification in the intestine. An excess of bile acids has a negative feedback effect, repressing further synthesis; conversely, when bile acids levels are low, synthesis is increased.2,6

In the ‘neutral’ pathway, the rate-limiting step is the modification of the steroid nucleus, which takes place in hepatic microsomes and is catalysed by cholesterol 7α-hydroxylase (CYP7A1). The neutral pathway facilitates the transformation of cholesterol to cholic acid and chenodeoxycholic acid, which are further conjugated to glycine or taurine and used as substrates for the bile acid transport pump. The canalicular transport of bile acid is the rate-limiting step of bile secretion. Bile acids are recovered from the intestines by the apical sodium-dependent bile acid transporter and return to the liver via the portal blood. The gene encoding CYP7A1 is highly regulated by negative feedback involving farnesoid X receptor (FXR)-dependent induction of fibroblast growth factor 15/19 (FGF15/19) expression by bile acids in the enterocytes. FGF15/19 binds to the fibroblast growth factor receptor 4-β-klotho complex in hepatocytes, activating signalling pathways that transcriptionally repress CYP7A1 expression.2

Enterohepatic circulation of bile acids

Bile acids are mostly restricted to enterohepatic circulation, circulating between the liver, the biliary tree, the intestine, and the portal blood which returns them to the liver. Almost all (95%) the bile acids are recovered from the intestine, mostly in the ileum.1 The liver converts around 500 mg of cholesterol into bile acids per day. This accounts for 90% of the cholesterol that is actively metabolized by the body. The remaining 10% of cholesterol that is synthesised is biosynthesised from steroid hormones.6

Newly synthesised bile acids are secreted into the bile where they are transported to the lumen of the small intestine, where they act as lipid emulsifiers, solubilising nutrients. These nutrients are incorporated into lipoproteins, and are delivered via the portal vein to the liver and metabolised. About 95% of the bile acids are recycled and secreted back into the bile. The remaining 5% are excreted into the faeces.6-7

Enterohepatic circulation of bile acids

adapted from van Mil 20057

ENTEROHEPATIC CYCLE

1. Monte MJ, Marin JJG, Antelo A, Vazquez-Tato J. Bile acids: chemistry, physiology, and pathophysiology. World J Gastroenterol 2009;15:804-16.

2. Jahnel J, Zöhrer E, Fischler B, et al. Attempt to determine the prevalence of two inborn errors of primary bile acid synthesis: results of a European survey. J Pediatr Gastroenterol Nutr 2017;64:864-8.

3. Sundaram SS, Bove KE, Lovell MA, Sokol RJ. Mechanisms of disease: Inborn errors of bile acid synthesis. Nat Clin Pract Gastroenterol Hepatol 2008;5:456-68.

4. Ashby K, Navarro Almario EE, Tong W, Borlak J, Mehta R, Chen M. Review article: therapeutic bile acids and the risks for hepatotoxicity. Aliment Pharmacol Ther 2018;47:1623-38.

5. Clayton PT. Disorders of bile acid synthesis. J Inherit Metab Dis 2011;34:593-604.

6. Russell DW. The enzymes, regulation, and genetics of bile acid synthesis. Annu Rev Biochem 2003;72:137-74.

7. van Mil SW, Houwen RH, Klomp LW. Genetics of familial intrahepatic cholestasis syndromes. J Med Genet 2005;42:449-63.

​TH-BAS10EN/01/02/2024

Normal values:

Vitamin A: 1,09-3,07 μmol/L

Vitamin E: 25-42 μmol/L

AST: <39 U/L

ALT: <34 U/L

GGT: <38 U/L

Total bilirubin: <17 μmol/L

Conjugated bilirubin level: <5 μmol/L

Normal values:

AST: < 45 mU/mL

International normalized ratio: < 1.2

Prothrombin ratio: 70-120 %

Factor VII: 70-120 %

Factor X: 70-120 %

Vitamin E: 300-1200 μg/dL

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Causes of jaundice in newborn or infant5

Jaundice of the newborns or infants

Unconjugated hyperbilirubinaemia

Mechanical haemolysis

Other causes of haemolysis

Intramedullary haemolysis

Infection-related haemolysis

Immune haemolysis

Constitutional haemolysis

Haemolysis

Default in the conjugation of
indirect bilirubin (UGT1A gene)

Rare genetic deficiency of canalicular
or sinusoidal specific transporter of
conjugated bilirubin

Moderate or severe hereditary
deficiency of enzyme activity

Enzyme immaturity or
enzymatic inhibition

Hepatocellular insufficiency

Cholestasis (decreased bile flow)

Other (hypothyroidism, trisomy 21)

Conjugated hyperbilirubinaemia

​TH-BAS07EN/01/02/2024

Bilirubin metabolism5-7

Important things to check: the degree and duration of stool discolouration. The colour of the stool should ideally be recorded after elimination of any component likely to change the colour and with the help of a colour chart:2, 14

This chart is used with the kind permission of the AMFE, Association Maladies Foie Enfants, a French association dedicated to liver diseases in children.3

You can also refer to the stool chart provided by the Children’s Liver Disease Foundation (CLDF), a UK charity committed to fighting all childhood liver diseases :

CLDF-Yellow-Alert-Stool-Chart

Persistently pale coloured stools may indicated liver disease.14  Complete and prolonged discolouration of stools for 7 days is suggestive of biliary atresia until proven otherwise. However, the sign is not specific to biliary atresia and can also occur, among others, in conditions such as cystic fibrosis, Alagille syndrome, alpha-1 antitrypsin deficiency and neonatal sclerosing cholangitis.2

​TH-BAS08EN/01/02/2024

What causes (rare) cholestasis
in paediatric patients

?

Menu

To access the platform and the
diagnostic algorithms,
please confirm:

If you are not a healthcare professional, please do not access the website as the content is not suitable. We invite you to continue your research through another website

Created by

Created by

Content reviewed by experts in paediatric gastroenterology and hepatology.

This website was created by Theravia. Theravia is a leading international pharmaceutical laboratory specializing in rare or neglected diseases. Formed through the merger of Addmedica and CTRS, we are dedicated to address the unmet medical needs of patients with these challenging conditions

03/2024

What causes (rare) cholestasis
in paediatric patients ?

Menu

To access the platform and the
diagnostic algorithms,
please confirm:

If you are not a healthcare professional, please do not access the website as the content is not suitable.
We invite you to continue your research through another website

This website was created by Theravia. Theravia is a leading international pharmaceutical laboratory specializing in rare or neglected diseases. Formed through the merger of Addmedica and CTRS, we are dedicated to address the unmet medical needs of patients with these challenging conditions

Created by

Content reviewed by experts in paediatric gastroenterology and hepatology.